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Trends Mol Med. 2013 Oct;19(10):604-13. doi: 10.1016/j.molmed.2013.08.001. Epub 2013 Sep 2.

Nuclear factor kappa B (NF-κB) in multiple sclerosis pathology.

Author information

1
Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, B-9052 Ghent, Belgium.

Abstract

The nuclear factor kappa B (NF-κB) signaling cascade plays a critical role in the regulation of immune and inflammatory responses and has been implicated in the pathogenesis of autoimmune demyelinating diseases such as multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), the main animal model of MS. NF-κB is essential for peripheral immune cell activation and the induction of pathology, but also plays crucial roles in resident cells of the central nervous system (CNS) during disease development. Here we review recent evidence clarifying the role of NF-κB in the different cell compartments contributing to MS pathology and its implications for the development of therapeutic strategies for the treatment of MS and other demyelinating pathologies of the CNS.

KEYWORDS:

NF-κB; Th17; cuprizone; demyelination; experimental autoimmune encephalomyelitis; multiple sclerosis

PMID:
24007818
DOI:
10.1016/j.molmed.2013.08.001
[Indexed for MEDLINE]

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